中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2010年
47期
3371-3375
,共5页
宫颈肿瘤%HeLa细胞%芍药属%细胞凋亡
宮頸腫瘤%HeLa細胞%芍藥屬%細胞凋亡
궁경종류%HeLa세포%작약속%세포조망
Cervical neoplasms%HeLa cells%Paeonia%Cell apoptosis
目的 探讨芍药苷对人子宫颈癌HeLa细胞增殖和凋亡的影响.方法 不同浓度芍药苷作用于人宫颈癌HeLa细胞后,采用四甲基偶氮唑蓝(MTT)比色法检测不同时间HeLa细胞的生长抑制效应,膜联蛋白V-异硫氰酸荧光素(FITC)/碘化丙啶(PI)双染色流式细胞术检测HeLa细胞凋亡率及细胞周期变化,透射电镜观察HeLa细胞形态变化,免疫细胞化学法检测芍药苷作用后HeLa细胞Bcl-2、Bax及Caspase-3表达的变化.结果 不同浓度的芍药苷作用不同时间后,对子宫颈癌HeLa细胞的生长抑制率呈明显的浓度-时间依赖关系,在24、48、72 h的IC50值分别为5054、2965、2459 μg/ml(P＜0.05);应用不同浓度芍药苷后HeLa细胞凋亡率逐渐增高,对照组及1000、2000μg/ml组凋亡率分别为0.94%、10.94%、13.95%(P＜0.05),细胞周期S期比例呈增多趋势;芍药苷作用48 h后透射电镜下可见HeLa细胞出现典型凋亡改变;芍药苷作用于HeLa细胞48 h后,与对照组相比Bcl-2表达减少、Bax及Caspase-3表达增多(P＜0.05).结论 芍药苷能够诱导子宫颈癌HeLa细胞凋亡,其作用机制可能与抗凋亡基因Bcl-2表达减弱及促凋亡基因Bax、Caspase-3表达增强有关.
目的 探討芍藥苷對人子宮頸癌HeLa細胞增殖和凋亡的影響.方法 不同濃度芍藥苷作用于人宮頸癌HeLa細胞後,採用四甲基偶氮唑藍(MTT)比色法檢測不同時間HeLa細胞的生長抑製效應,膜聯蛋白V-異硫氰痠熒光素(FITC)/碘化丙啶(PI)雙染色流式細胞術檢測HeLa細胞凋亡率及細胞週期變化,透射電鏡觀察HeLa細胞形態變化,免疫細胞化學法檢測芍藥苷作用後HeLa細胞Bcl-2、Bax及Caspase-3錶達的變化.結果 不同濃度的芍藥苷作用不同時間後,對子宮頸癌HeLa細胞的生長抑製率呈明顯的濃度-時間依賴關繫,在24、48、72 h的IC50值分彆為5054、2965、2459 μg/ml(P＜0.05);應用不同濃度芍藥苷後HeLa細胞凋亡率逐漸增高,對照組及1000、2000μg/ml組凋亡率分彆為0.94%、10.94%、13.95%(P＜0.05),細胞週期S期比例呈增多趨勢;芍藥苷作用48 h後透射電鏡下可見HeLa細胞齣現典型凋亡改變;芍藥苷作用于HeLa細胞48 h後,與對照組相比Bcl-2錶達減少、Bax及Caspase-3錶達增多(P＜0.05).結論 芍藥苷能夠誘導子宮頸癌HeLa細胞凋亡,其作用機製可能與抗凋亡基因Bcl-2錶達減弱及促凋亡基因Bax、Caspase-3錶達增彊有關.
목적 탐토작약감대인자궁경암HeLa세포증식화조망적영향.방법 불동농도작약감작용우인궁경암HeLa세포후,채용사갑기우담서람(MTT)비색법검측불동시간HeLa세포적생장억제효응,막련단백V-이류청산형광소(FITC)/전화병정(PI)쌍염색류식세포술검측HeLa세포조망솔급세포주기변화,투사전경관찰HeLa세포형태변화,면역세포화학법검측작약감작용후HeLa세포Bcl-2、Bax급Caspase-3표체적변화.결과 불동농도적작약감작용불동시간후,대자궁경암HeLa세포적생장억제솔정명현적농도-시간의뢰관계,재24、48、72 h적IC50치분별위5054、2965、2459 μg/ml(P＜0.05);응용불동농도작약감후HeLa세포조망솔축점증고,대조조급1000、2000μg/ml조조망솔분별위0.94%、10.94%、13.95%(P＜0.05),세포주기S기비례정증다추세;작약감작용48 h후투사전경하가견HeLa세포출현전형조망개변;작약감작용우HeLa세포48 h후,여대조조상비Bcl-2표체감소、Bax급Caspase-3표체증다(P＜0.05).결론 작약감능구유도자궁경암HeLa세포조망,기작용궤제가능여항조망기인Bcl-2표체감약급촉조망기인Bax、Caspase-3표체증강유관.
Objective To explore the effects of paeoniflorin on the proliferation and apoptosis of HeLa cells. Methods HeLa cells treated with paeoniflorin at different concentrations for different hours were assessed by the method of methyl thiazolyl tetrazolium (MTT). Cell apoptosis rate and cycle change were detected by flow cytometry with annexin V-fluorescein isothiocvanate (FITC)/propidium iodide (PI). The morphological change of HeLa cells was observed by transmission electron microscope (TEM). The expressions of Bcl-2, Bax and Caspase-3 in HeLa cells induced by paeoniflorin were detected by immunocytochemistry. Results After treatment with different concentrations of paeoniflorin for different hours, the proliferation of HeLa cells was inhibited in a dose and time-dependent manner with an IC50 value of 5054, 2965, 2459 μg/ml at 24, 48 and 72 hours respectively (P ＜ 0. 05). After treated by different concentrations of paeoniflorin (control group, 1000 and 2000 μg/ml), apoptosis was induced in HeLa cells at a rate of 0. 94%, 10. 94% and 13.95% respectively. Such effects were dose-dependent (P ＜0. 05) and the proportion of HeLa cells in Sphase was under a rising trend. Typical apoptotic changes of HeLa cells under the exposure to paeoniflorin were observed under TEM. There was a lowered expression of Bcl-2 and an elevated expression of Bax and Caspase-3 genes versus the control group after a 48-hour paeoniflorin treatment (P ＜ 0. 05). Conclusion Paeoniflorin can significantly induce the apoptosis of HeLa cells through a down-regulation of anti-apoptotic gene Bcl-2 and an up-regulation of pro-apoptotic genes Bax and Caspase-3.
